Document Detail


A direct role for C1 inhibitor in regulation of leukocyte adhesion.
MedLine Citation:
PMID:  15879149     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Plasma C1 inhibitor (C1INH) is a natural inhibitor of complement and contact system proteases. Heterozygosity for C1INH deficiency results in hereditary angioedema, which is mediated by bradykinin. Treatment with plasma C1INH is effective not only in patients with hereditary angioedema, but also in a variety of other disease models, in which such therapy is accompanied by diminished neutrophil infiltration. The underlying mechanism has been explained primarily as a result of the inhibition of the complement and contact systems. We have shown that C1INH expresses the sialyl-Lewis(x) tetrasaccharide on its N-linked glycan, via which it binds to E- and P-selectins and interferes with leukocyte-endothelial adhesion in vitro. Here we show that both native C1INH and reactive center cleaved C1INH significantly inhibit selectin-mediated leukocyte adhesion in several in vitro and in vivo models, whereas N-deglycosylated C1INH loses such activities. The data support the hypothesis that C1INH plays a direct role in leukocyte-endothelial cell adhesion, that the activity is mediated by carbohydrate, and that it is independent of protease inhibitory activity. Direct involvement of C1INH in modulation of selectin-mediated cell adhesion may be an important mechanism in the physiologic suppression of inflammation, and may partially explain its utility in therapy of inflammatory diseases.
Authors:
Shenghe Cai; Vandana S Dole; Wolfgang Bergmeier; Jennifer Scafidi; Hanping Feng; Denisa D Wagner; Alvin E Davis
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  174     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  2005 May 
Date Detail:
Created Date:  2005-05-09     Completed Date:  2005-07-05     Revised Date:  2014-09-22    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  6462-6     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
CHO Cells
Carcinoembryonic Antigen / metabolism
Cell Adhesion / immunology
Cell Migration Inhibition
Complement C1 Inactivator Proteins / physiology*
Complement Pathway, Classical
Cricetinae
E-Selectin / metabolism
Endothelium, Vascular / cytology,  immunology
HL-60 Cells
Humans
Leukocyte Rolling / immunology
Leukocytes / cytology*,  enzymology,  immunology*
Ligands
Mice
Mice, Inbred BALB C
Neutrophil Infiltration / immunology
Peritonitis / chemically induced,  immunology,  pathology
Thioglycolates / administration & dosage
Grant Support
ID/Acronym/Agency:
P01 HL056949/HL/NHLBI NIH HHS; P01-HL56949/HL/NHLBI NIH HHS; R01-HD033727/HD/NICHD NIH HHS; R37 HL041002/HL/NHLBI NIH HHS; R37-HD22082/HD/NICHD NIH HHS; R37-HL-41002/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Carcinoembryonic Antigen; 0/Complement C1 Inactivator Proteins; 0/E-Selectin; 0/Ligands; 0/Thioglycolates

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